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The OmicShare tools platform is a user‐friendly online resource for data analysis and visualization, encompassing 161 bioinformatic tools. Users can easily track the progress of projects in real‐time through an overview interface. The platform has a powerful interactive graphics engine that allows for the custom‐tailored modification of charts generated from analyses. The visually appealing charts produced by OmicShare improve data interpretability and meet the requirements for publication. It has been acknowledged in over 4000 publications and is available in https://www.omicshare.com/tools/.

Background The triglyceride glucose (TyG) index has been proposed as a reliable marker of insulin resistance (IR) and an independent predictor of cardiovascular disease risk. However, its prognostic value in patients with acute decompensated heart failure (ADHF) remains unclear. Methods A total of 932 hospitalized patients with ADHF from January 1st, 2018 to February 1st, 2021 were included in this retrospective study. The TyG index was calculated as ln [fasting triglyceride level (mg/dL) × fasting plasma glucose level (mg/dL)/2]. Patients were divided into tertiles according to TyG index values. The primary endpoints were all-cause death, cardiovascular (CV) death and major adverse cardiac and cerebral events (MACCEs) during follow-up. We used multivariate adjusted Cox proportional hazard models and restricted cubic spline analysis to investigate the associations of the TyG index with primary endpoints. Results During a median follow-up time of 478 days, all-cause death, CV death and MACCEs occurred in 140 (15.0%), 103 (11.1%) and 443 (47.9%) cases, respectively. In multivariate Cox proportional hazard models, the risk of incident primary endpoints was associated with the highest TyG tertile. After adjustment for confounding factors, hazard ratios (HRs) for the highest tertile (TyG index ≥ 9.32) versus the lowest tertile (TyG index < 8.83) were 2.09 (95% confidence interval [CI], 1.23–3.55; p = 0.006) for all-cause death, 2.31 (95% CI, 1.26–4.24; p = 0.007) for CV death and 1.83 (95% CI, 1.18–3.01; p = 0.006) for MACCEs. Restricted cubic spline analysis also showed that the cumulative risk of primary endpoints increased as TyG index increased. When the TyG index was used as a continuous variable, the hazard ratios of the three primary endpoints rapidly increased within the higher range of the TyG index (all cause death, TyG > 9.08; CV death, TyG > 9.46; MACCEs, TyG > 9.87). Conclusions The elevated TyG index was independently associated with poor prognosis, and thus would be useful in the risk stratification in patients with ADHF.

Regulation of the programming of tumour-associated macrophages (TAMs) controls tumour growth and anti-tumour immunity. We examined the role of FGF2 in that regulation. Tumours in mice genetically deficient in low-molecular weight FGF2 (FGF2 LMW ) regress dependent on T cells. Yet, TAMS not T cells express FGF receptors. Bone marrow derived-macrophages from Fgf2 LMW−/− mice co-injected with cancer cells reduce tumour growth and express more inflammatory cytokines. FGF2 is induced in the tumour microenvironment following fractionated radiation in murine tumours consistent with clinical reports. Combination treatment of in vivo tumours with fractionated radiation and a blocking antibody to FGF2 prolongs tumour growth delay, increases long-term survival and leads to a higher iNOS + /CD206 + TAM ratio compared to irradiation alone. These studies show for the first time that FGF2 affects macrophage programming and is a critical regulator of immunity in the tumour microenvironment. Macrophages contribute to tumour progression and response to therapy. Here, the authors show that absence of FGF2 in the tumour microenvironment reduces tumour growth and enhances the anti-tumour immune response by altering macrophage polarization. As a result, disruption of this macrophage programming by anti-FGF2 blocking antibodies enhances the outcome from radiotherapy. 

The purpose of this research was to evaluate the effectiveness and safety of neoadjuvant chemotherapy plus radical surgery (NCRS) and concurrent chemoradiotherapy (CCRT) based on three-dimensional conformal radiation therapy (3DCRT) for FIGO 2018 stage IB3/IIA2 patients with cervical squamous cell carcinoma in a resource-limited setting. The clinical outcomes and incidence of complications in 137 patients who underwent NCRS with those of 163 patients who CCRT based on 3DCRT were compared. Propensity score matching (PSM) analysis was used to match the two groups to enable further statistical comparisons. Survival analysis was performed utilizing Cox proportional hazards regression analyses, Kaplan-Meier curves, and log-rank tests. Furthermore, the incidence of complications between the two groups was also compared using chi-squared tests. PSM analysis identified 103 matched pairs of patients. The NCRS and CCRT groups exhibited 5-year overall survival (OS) rates of 85.4% and 91.2%, respectively (p=0.19). Additionally, the NCRS and CCRT groups exhibited 5-year disease-free survival (DFS) rates of 76.7% and 89.3% (p=0.02), and the recurrence rates were 20.4% and 9.7% (p=0.03), respectively. However, the CCRT group exhibited a higher incidence of early any-grade complications (79.6% vs 35.9%, p<0.001) and early grade 3 complications (15.5% vs 2.9%, p=0.002) compared to the NCRS group. In terms of overall late complications, there was no significant difference in the incidence between the two groups. Multivariate analysis revealed that stage IIA2 emerged as an independent risk factor for OS (aHR 8.89; p=0.033). Moreover, histologic grade 2-3 (aHR 5.3; p=0.022), stage IIA2 (aHR 2.95; p=0.043), NCRS treatment (aHR 2.41; p=0.012) were identified as independent risk factors for DFS. In resource-limited settings, for patients with FIGO 2018 stage IB3/IIA2 cervical squamous cell carcinoma, 3DCRT-based CCRT offers superior disease-free survival and reduced recurrence rates compared to NCRS, despite increased early complication rates.

Background Circulating fibrinogen-to-albumin ratio (FAR) has been proposed as a novel inflammatory biomarker and a cardiovascular disease risk predictor. However, its prognostic value in patients with acute decompensated heart failure (ADHF) and different glycemic metabolic states remains ambiguous. Methods A total of 1031 hospitalized patients with ADHF from January 2018 to May 2021 were included in the study. The primary endpoints were the major adverse cardiac and cerebral events (MACCEs). Patients were categorized into high-level FAR (FAR-H) and low-level FAR (FAR-L) groups based on the optimal cut-off value of FAR obtained from restricted cubic spline function analysis. The Kaplan–Meier plots and three multivariate-adjusted Cox proportional hazard models were used to determine the association between FAR and the risk of developing MACCEs in patients with ADHF at different glycemic metabolic states. Results MACCEs occurred in 483 (46.8%) patients during a median follow-up time of 520 days. The optimal FAR cut-off value was 0.079. Upon analyzing the Kaplan–Meier plots, the incidence of MACCEs was significantly different between the FAR groups in all patients and patients with diabetes mellitus (p < 0.05). After adjusting for the confounding factors, the hazard ratio (HR) for MACCEs in the FAR-H group was 1.29 compared with the FAR-L group in all patients (Model 3: 95% CI 1.07–1.56, p = 0.007). Additionally, high FAR was associated with MACCEs in three multivariate Cox models (Model 1, HR = 1.52, 95% CI 1.17–1.96, p = 0.002; Model 2, HR = 1.46, 95% CI 1.13–1.89, p = 0.004; Model 3, HR = 1.48, 95% CI 1.14–1.92, p = 0.003) in DM patients. But no significant differences were found between the FAR groups for prediabetes mellitus (Pre-DM) and normal glucose regulation (NGR) using the three Cox models (all p-values were > 0.05). Conclusions Elevated FAR was independently associated with poor prognosis in patients with ADHF and DM and thus could be used as a risk stratification tool and a potential therapeutic target in the future.

The growth of intelligent manufacturing systems has led to a wealth of computation-intensive tasks with complex dependencies. These tasks require an efficient offloading architecture that balances responsiveness and energy efficiency across distributed computing resources. Existing task offloading approaches have fundamental limitations when simultaneously optimizing multiple conflicting objectives while accommodating hierarchical computing architectures and heterogeneous resource capabilities. To address these challenges, this paper presents a cloud–fog hierarchical collaborative computing (CFHCC) framework that features fog cluster mechanisms. These methods enable coordinated, multi-node parallel processing while maintaining data sensitivity constraints. The optimization of task distribution across this three-tier architecture is formulated as a multi-objective problem, minimizing both system latency and energy consumption. To solve this problem, a fractal-based multi-objective optimization algorithm is proposed to efficiently explore Pareto-optimal task allocation strategies by employing recursive space partitioning aligned with the hierarchical computing structure. Simulation experiments across varying task scales demonstrate that the proposed method achieves a 20.28% latency reduction and 3.03% energy savings compared to typical and advanced methods for large-scale task scenarios, while also exhibiting superior solution consistency and convergence. A case study on a digital twin manufacturing system validated its practical effectiveness, with CFHCC outperforming traditional cloud–edge collaborative computing by 12.02% in latency and 11.55% in energy consumption, confirming its suitability for diverse intelligent manufacturing applications.

Cancer stemness and osteosarcoma (OS) malignant progression are closely associated. However, the molecular mechanisms underlying this association have not been fully demonstrated. Long noncoding RNAs (lncRNAs) are an intriguing class of widely prevalent endogenous RNAs involved in OS progression, the vast majority of which have not been characterized functionally. Here, we identified tumor promoter lncRNA WAC-AS1 to be highly expressed in OS tumors and associated with worse survival. Further analysis revealed that WAC-AS1 increased tumorsphere formation of OS cells and promoted metastasis, as confirmed by cell proliferation, transwell and wound healing assays. MiR-5047 was identified as a downstream target of WAC-AS1. Subsequently, based on bioinformatics analysis, RIP assay and luciferase reporter assay, SOX2 mRNA was verified as a target of miR-5047. WAC-AS1 enhanced OS cell proliferation and stemness via acting as a ceRNA by binding to miR-5047, thereby increasing SOX2 expression. In addition, SOX2 bound to the promoter region of WAC-AS1 and promoted its transcription, thereby forming a positive feedback loop to regulate OS malignancy. Taken together, our findings show WAC-AS1 is a tumor promoter and a key regulator of OS cell stemness and metastasis via a miR-5047/SOX2 axis.

Background Cardiovascular diseases (CVDs) are a significant cause of mortality worldwide and are characterized by severe atherosclerosis (AS) in patients. However, the molecular mechanism of AS formation remains elusive. In the present study, we investigated the role of syndecan-4 (SDC4), a member of the syndecan family, in atherogenesis. Methods and Results The expression of SDC4 decreased in mouse severe AS models. Moreover, knockout of SDC4 accelerated high-cholesterol diets (HCD)-induced AS in ApoE −/− mice. Mechanistically, the decrease of SDC4 increased macrophage proinflammatory capacity may be through the PKCα-ABCA1/ABCG1 signaling pathway. Conclusion These findings provide evidence that SDC4 reduction links macrophages and inflammation to AS and that SDC4 in macrophages provides a therapeutic target for preventing AS formation.

Background The present study was performed to assess the association between the neutrophil-to-apolipoprotein A1 ratio (NAR) and outcomes in patients with acute decompensated heart failure (ADHF) at different glucose metabolism states. Methods We recruited 1233 patients with ADHF who were admitted to Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University from December 2014 to October 2019. The endpoints were defined as composites of cardiovascular death, nonfatal myocardial infarction, nonfatal ischemic stroke and exacerbation of chronic heart failure. The restricted cubic spline was used to determine the best cutoff of NAR, and patients were divided into low and high NAR groups. Kaplan-Meier plots and multivariable Cox proportional hazard models were used to investigate the association between NAR and the risk of adverse outcomes. Results During the five-year follow-up period, the composite outcome occurred in 692 participants (56.1%). After adjusting for potential confounding factors, a higher NAR was associated with a higher incidence of composite outcomes in the total cohort (Model 1: HR = 1.42, 95% CI = 1.22–1.65, P <0.001; Model 2: HR = 1.29, 95% CI = 1.10–1.51, P  = 0.002; Model 3: HR = 1.20, 95% CI = 1.01–1.42, P  = 0.036). At different glucose metabolic states, a high NAR was associated with a high risk of composite outcomes in patients with diabetes mellitus (DM) (Model 1: HR = 1.54, 95% CI = 1.25–1.90, P <0.001; Model 2: HR = 1.40, 95% CI = 1.13–1.74, P  = 0.002; Model 3: HR = 1.31, 95% CI = 1.04–1.66, P  = 0.022), and the above association was not found in patients with prediabetes mellitus (Pre-DM) or normal glucose regulation (NGR) (both P >0.05). Conclusions The NAR has predictive value for adverse outcomes of ADHF with DM, which implies that the NAR could be a potential indicator for the management of ADHF.

LMNA gene encodes lamin A/C protein which participates in the construction of nuclear lamina, the mutations of LMNA result in a wide variety of diseases known as laminopathies. LMNA-related dilated cardiomyopathy(LMNA-DCM) is one of the more common laminopathy which characterized by progressive heart failure and arrhythmia. However, the mutation features of LMNA-DCM are yet to be elucidated. Herein we described a dilated cardiomyopathy family carrying novel variant c.467G > C(p.Arg156Pro) of LMNA as heterozygous pathogenic variant identified by whole-exome sequencing. With the help of Alphafold2, we predicted mutant protein structure and found an interrupted α-helix region in lamin A/C. In the analysis of 49 confirmed pathogenic missense of laminopathies, Chi-square test showed the DCM phenotype was related to the α-helix region mutation (p < 0.017). After screening the differentially expressed genes (DEGs) in both mice models and human patients in Gene Expression Omnibus database, we found the variation of α-helix-coding region in LMNA caused abnormal transcriptomic features in cell migration, collagen-containing extracellular matrix, and PI3K-Akt signaling pathway. Subsequently we constructed (TF)-mRNA-microRNA (miRNA) regulatory network and identified 7 key genes ( FMOD , CYP1B1 , CA3 , F2RL1 , HAPLIN1 , SNAP91 , and KANSL1 ) as potential biomarkers or therapeutic targets in LMNA-DCM patients.